| ARID2, BAF200, p200, AT-rich interaction domain 2|
MGI: 1924294 HomoloGene: 14601 GeneCards: ARID2
AT-rich interactive domain-containing protein 2 (ARID2) is a protein that in humans is encoded by the ARID2 gene.
ARID2 is a subunit of the PBAF chromatin-remodeling complex, which facilitates ligand-dependent transcriptional activation by nuclear receptors.
The ARID2 protein contains two conserved C-terminal C2H2 zinc fingers motifs, a region rich in the amino acid residues proline and glutamine, a RFX (regulatory factor X)-type winged-helix DNA-binding domain, and a conserved N-terminal AT-rich DNA interaction domain—the last domain for which the protein is named.
Mutation studies have revealed ARID2 to be a significant tumor suppressor in many cancer subtypes. ARID2 mutations are prevalent in hepatocellular carcinoma and melanoma. Mutations are present in a smaller but significant fraction in a wide range of other tumors. ARID2 mutations are enriched in hepatitis C virus-associated hepatocellular carcinoma in the US and European patient populations compared with the overall mutation frequency.
The ARID2 gene, located on chromosome 12q in humans, consists of 21 exons; orthologs are known from mouse, rat, cattle, chicken, and mosquito. Model organisms have been used in the study of ARID2 function. A conditional knockout mouse line, called Arid2tm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program, a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty six tests were carried out on mutant adult mice and two significant abnormalities were observed. A recessive lethal study found fewer homozygous mutant embryos during gestation than predicted by Mendelian ratio. In a second study, no homozygous mutant animals survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice; these displayed no abnormalities.